CED-9 and mitochondrial homeostasis in C. elegans muscle. J Cell Sci 2008 Oct 15;121(Pt 20):3373-82
Date
10/02/2008Pubmed ID
18827010Pubmed Central ID
PMC2785848DOI
10.1242/jcs.032904Scopus ID
2-s2.0-56349100757 (requires institutional sign-in at Scopus site) 40 CitationsAbstract
Mitochondrial homeostasis reflects a dynamic balance between membrane fission and fusion events thought essential for mitochondrial function. We report here that altered expression of the C. elegans BCL2 homolog CED-9 affects both mitochondrial fission and fusion. Although striated muscle cells lacking CED-9 have no alteration in mitochondrial size or ultrastructure, these cells appear more sensitive to mitochondrial fragmentation. By contrast, increased CED-9 expression in these cells produces highly interconnected mitochondria. This mitochondrial phenotype is partially suppressed by increased expression of the dynamin-related GTPase DRP-1, with suppression dependent on the BH3 binding pocket of CED-9. This suppression suggests that CED-9 directly regulates DRP-1, a model supported by our finding that CED-9 activates the GTPase activity of human DRP1. Thus, CED-9 is capable of regulating the mitochondrial fission-fusion cycle but is not essential for either fission or fusion.
Author List
Tan FJ, Husain M, Manlandro CM, Koppenol M, Fire AZ, Hill RBMESH terms used to index this publication - Major topics in bold
AnimalsCaenorhabditis elegans
Caenorhabditis elegans Proteins
Dynamins
GTP Phosphohydrolases
Homeostasis
Humans
Membrane Fusion
Microtubule-Associated Proteins
Mitochondria
Mitochondrial Membranes
Mitochondrial Proteins
Models, Biological
Proto-Oncogene Proteins c-bcl-2
